The Raging Evolutionary War Between Humans and Covid-19

The race is turned on. Covid-19-causing virus vaccines are taking hold around the world, the tip of the hypodermic spear of a year-long scientific triumph. But this virus protean, like all things that infect humans and make them sick, shock and dodge.

Virology versus epidemiology. Vaccinology versus evolution. Mutation versus mutation, transmission against infection, virus versus vaccine. To start! Yours! Motors! Last year (horrible, tragic, not good, very bad) could have seemed like a direct battle between scientists and a virus to find new drugs and vaccines. But this was not just a foot fight; it was also a bug hunt: a subtle boost through a dozen different vectors. Viruses are not exactly alive, but they follow the same rulebook as all living things on Earth: adapt or die. Understanding these more hidden forces, how viruses evolve within us, their hosts, and how they change from one person to the next, will define the next phase of the pandemic.

It is easy to find out the new variants of the SARS-CoV-2 virus, with its science fiction nomenclature. There is B.1.1.7, which seems to be a fad when it comes to infecting new people. And you have B.1.351 and P.1, perhaps not better at host-to-host transmission, but better at eluding an immune response (natural, or the type that a vaccine induces). A lot of those who escape immunity share the same mutation, even if they are only remotely related. That, as the saying goes, is life. “The way the virus evolves, the foundations of evolution, are the same. What is different is that it is played on a very, very large scale. There are so many infected people and each person has many viruses. So there are a lot of opportunities for the virus to make mutations and try new things, ”says Adam Lauring, a virologist at the University of Michigan who studies viral evolution. “From time to time, one of them takes off. It is an uncommon fact, but when the virus has so many opportunities to solve it, it will happen with increasing frequency. It is both a game of epidemiology, that is, and evolutionary biology.

So even though it may seem like these variants have some sort of malicious intent — to make people sick, to kill all humans! “It’s not what’s happening.” Viruses want nothing; they are only verbs. Infect, reproduce, infect. A virus that kills too efficiently doesn’t become a virus for long, as dead guests can’t walk around breathing with uninfected but susceptible suckers. Therefore, one hypothesis says that these successful mutations are primarily changes in the way the virus infects. That is, they improve the way the virus enters a human being or enters a human cell or reproduces in that cell (because the more virus a person produces, the more it releases and the more likely it is to reach someone else).

This is probably why all these similar variants seem to emerge at once and quickly. Viruses are just small jets of protein wrapped around large molecules of code, of genetic material. In SARS-CoV-2, this material is RNA. And some viruses produce mutations more often than others.

Viruses evolve because they reproduce (in fact, it’s almost all their part) and errors are introduced into this genetic material in the process. Over the generations, sometimes these random or “stochastic” mistakes really make the virus do its thing better; sometimes they make it worse. That is, the life circumstances or way of life of a virus is played against random changes in the code underlying its genes. (SARS-CoV-2 appears to mutate at approximately the same rate as other RNA viruses, although, like other coronaviruses in its family, it has a built-in error correction mechanism. It needs it, because its genome is so large, relatively speaking — three times the size of the HIV genome, the virus that causes AIDS, for example. “Without the correction, too many mutations would probably be created per virus replication event to remain viable,” says Katrina Lythgoe , an evolutionary epidemiologist at the Big Data Institute at Oxford University (this type of genomic suicide is called crossing the “threshold of error catastrophe”).

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